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• Abnormal serum creatinine (1.6 mg/dL) and creatinine clearance (33 mL/min) levels found in a 50-year-old woman during fasting were corrected with refeeding. Five healthy subjects who fasted for 96 hours demonstrated an increase in their mean serum creatinine level from 1.0±0.08 to 1.7±0.11 mg/dL as determined by Jaffe's method. This increase was probably an artifact caused by the rise in the serum acetoacetate level during fasting. The serum creatinine level determined by an enzymatic method and serum urea nitrogen level did not change substantially during the fast. We conclude that fasting may cause an artifactual increase in the serum creatinine level determined by Jaffe's method, the method used by most clinical laboratories. ( Arch Intern Med 1984;144:1575-1576)

To learn more about the metabolic effects of dietary fructose and sucrose, 12 type I and 12 type II diabetic subjects were fed three isocaloric (or isoenergic) diets for eight days each according to a randomized, crossover design. The three diets provided, respectively, 21% of the energy as fructose, 23% of the energy as sucrose, and almost all carbohydrate energy as starch. The fructose diet resulted in significantly lower one- and two-hour postprandial plasma glucose levels, overall mean plasma glucose levels, and urinary glucose excretion in both type I and type II subjects than did the starch diet. There were no significant differences between the sucrose and starch diets in any of the measures of glycemic control in either subject group. The fructose and sucrose diets did not significantly increase serum triglyceride values when compared with the starch diet, but both increased postprandial serum lactate levels. We conclude that short-term replacement of other carbohydrate sources in the diabetic diet with fructose will improve glycemic control, whereas replacement with sucrose will not aggravate glycemic control.

Of 11 patients with active acromegaly treated with transsphenoidal selective pituitary adenomectomy, four failed to show evidence of clinical improvement. An additional four patients showed clinical and biochemical improvement after the surgical procedure but, with more prolonged follow-up, showed a recurrence of acromegaly. Only three patients had prolonged clinical and biochemical evidence of improvement; they had glucose suppressed growth hormone concentrations of 1.0, 2.7, and 2.8 ng/mL 22, 40, and 24 months, respectively, after the surgical procedure. Two of these three patients, however, showed an increase in growth hormone concentration after thyrotropin-releasing hormone injection, a finding that suggests the possibility of eventual relapse. Our data also clearly indicated a need for more rigorous criteria for biochemical cure of acromegaly than those used previously. Study of 20 healthy volunteers showed that growth hormone concentration should normally be suppressible to less than 2.0 ng/mL after 100 g oral glucose.

• Five patients from two unrelated families were found to have goiter and elevated serum concentrations of thyroxine (T 4 ) and triiodothyronine (T 3 ) without symptoms or signs of hyperthyroidism. All had measurable concentrations of thyroid stimulating hormone (TSH), and in four who were tested, there was an increase in TSH concentration following thyrotropin releasing hormone (TRH) administration. We believe these five patients have general resistance to the effects of thyroid hormones and need elevated concentrations of T 4 and T 3 to maintain a eumetabolic state. Study of nuclear T 3 receptors from cultured fibroblasts of one patient disclosed a normal equilibrium association constant and a maximal binding capacity that was greater than normal control values. These findings suggest that thyroid hormone resistance in this patient is not due to a decrease in either the affinity or the number of specific nuclear T 3 receptors. This disorder can easily be confused with Graves' disease and result in inappropriate treatment for hyperthyroidism, as was the case in three of our patients. ( Arch Intern Med 1982;142:1867-1871)

To evaluate the mechanism of cyclosporine-induced hyperkalemia, the renin-angiotensin-aldosterone system and renal potassium clearance were compared in ten renal transplant recipients treated with cyclosporine and treated with azathioprine. After stimulation by a low-sodium diet and furosemide, cyclosporine-treated patients demonstrated lower plasma renin activity when supine (1.9 +/- 0.3 v 7.8 +/- 1.4 ng/mL/hr) and after standing (3.0 +/- 0.7 v 12.2 +/- 1.5 ng/mL/hr). Supine plasma aldosterone levels tended to be lower in cyclosporine-treated patients, (4.8 +/- v 10.5 +/- 2.6 ng/dL), although standing plasma aldosterone levels were not different (10.8 +/- 3.0 v 12.3 +/- 2.0 ng/dL). After administration of 0.75 mEq of potassium chloride per kilogram of body weight, cyclosporine-treated patients excreted 52% +/- 7.1% of the potassium load in six hours compared with excretion of 67% +/- 7.0% by the azathioprine-treated patients, although there was no difference in plasma aldosterone levels in response to the potassium load in the two groups. These data suggest that cyclosporine causes suppression of plasma renin activity and a tubular insensitivity to aldosterone, both of which may impair potassium excretion.